FLT3, is a promising therapeutic target for leukemia and is mutated in approximately ⅓ of AML patients. Of growing concern, however, is the development of drug resistance resulting from the emergence of point mutations in targeted tyrosine kinases used for the treatment of acute leukemia patients. See Shah et al. (2002) and Cools et al. (2003). One approach to overriding such resistance is to combine structurally unrelated inhibitors and/or inhibitors of different signaling pathways.